[Federal Register: September 29, 2003 (Volume 68, Number 188)]
[Rules and Regulations]
[Page 55833-55849]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr29se03-20]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 180
[OPP-2003-0058; FRL-7327-9]
Glufosinate Ammonium; Pesticide Tolerance
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
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SUMMARY: This regulation establishes a tolerance for combined residues
of glufosinate ammonium and its metabolites in or on certain raw
agricultural commodities. Aventis CropScience USA, now Bayer
CropScience, and Interregional Research Project Number 4 (IR-4)
requested these tolerances under the Federal Food, Drug, and Cosmetic
Act (FFDCA), as amended by the Food Quality Protection Act of 1996
(FQPA).
DATES: This regulation is effective September 29, 2003. Objections and
requests for hearings, identified by docket ID number OPP-2003-0058,
must be received on or before November 28, 2003.
ADDRESSES: Written objections and hearing requests may be submitted
electronically, by mail, or through hand delivery/courier. Follow the
detailed instructions as provided in Unit VI. of the SUPPLEMENTARY
INFORMATION.
FOR FURTHER INFORMATION CONTACT: Joanne I. Miller, Registration
Division (7505C), Office of Pesticide Programs, Environmental
Protection Agency, 1200 Pennsylvania Ave., NW.,Washington, DC 20460-
0001; telephone number: 703-305-6224; e-mail address: miller.joanne@epamail.epa.gov.
SUPPLEMENTARY INFORMATION:
I. General Information
A. Does this Action Apply to Me?
You may be potentially affected by this action if you are an
agricultural producer, food manufacturer, or pesticide manufacturer.
Potentially affected categories and entities may include, but are not
limited to:
[bull] Crop production (NAICS 111)
[bull] Animal production (NAICS 112)
[bull] Food manufacturing (NAICS 311)
[bull] Pesticide manufacturing (NAICS 32532)
This listing is not intended to be exhaustive, but rather provides
a guide for readers regarding entities likely to be affected by this
action. Other types of entities not listed in the table could also be
affected. The North American Industrial Classification System (NAICS)
codes have been provided to assist you and others in determining
whether or not this action might apply to certain entities. If you have
questions regarding the applicability of this action to a particular
entity, consult the person listed under FOR FURTHER INFORMATION
CONTACT.
B. How Can I Get Copies of this Document and Other Related Information?
1. Docket. EPA has established an official public docket for this
action under docket identification (ID) number OPP-2003-0058. The
official public docket consists of the documents specifically
referenced in this action, any public comments received, and other
information related to this action. Although a part of the official
docket, the public docket does not include Confidential Business
Information (CBI) or other information whose disclosure is restricted
by statute. The official public docket is the collection of materials
that is available for public viewing at the Public Information and
Records Integrity Branch (PIRIB), Rm. 119, Crystal Mall 2,
1921 Jefferson Davis Hwy., Arlington, VA. This docket facility is open
from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal
holidays. The docket telephone number is (703) 305-5805.
2. Electronic access. You may access this Federal Register document
electronically through the EPA Internet under the ``Federal Register''
listings at http://www.epa.gov/fedrgstr/http://.
http://www.access.gpo.gov/nara/cfr/cfrhtml_00/Title_40/40cfr180_00.html/, a
beta site currently under development. To access the OPPTS Harmonized
Guidelines referenced in this document, go directly to the guidelines
at http://www.epa.gov/opptsfrs/home/guidelin.htm.
An electronic version of the public docket is available through
EPA's electronic public docket and comment system, EPA Dockets. You may
use EPA Dockets at http://www.epa.gov/edocket/ to submit or view public
comments, access the index listing of the contents of the official
public docket, and to access those documents in the public docket that
are available electronically. Although not all docket materials may be
available electronically, you may still access any of the publicly
available docket materials through the docket facility identified in
Unit I.B.1. Once in the system, select ``search,'' then key in the
appropriate docket ID number.
II. Background and Statutory Findings
In the Federal Register of May 19, 2000 (65 FR 31904) (FRL-6558-2),
EPA issued a notice pursuant to section 408 of FFDCA, 21 U.S.C. 346a,
as amended by FQPA (Public Law 104-170), announcing the filing of a
pesticide petition (PP 0F6140) by Aventis CropScience USA, now Bayer
CropScience, PO Box 12014, 2 T. W. Alexander Drive, Research Triangle
Park, NC 27709. That notice included a summary of the petition prepared
by Bayer CropScience, the registrant. There were no comments received
in response to the notice of filing.
In the Federal Register of July 24, 2002 (67 FR 48465) (FRL-7184-
6), EPA issued a notice pursuant to section 408 of FFDCA, 21 U.S.C.
346a, as amended by FQPA (Public Law 104-170), announcing the filing of
a pesticide petition (PP OF6210) by Aventis CropScience USA, now Bayer
CropScience, PO Box 12014, 2 T. W. Alexander Drive, Research Triangle
Park, NC 27709. That notice included a summary of the petition prepared
by Bayer CropScience, the registrant. Comments on the petition were
filed by Neil J. Carman, Ph.D. of the Sierra Club
[[Page 55834]]
Genetic Engineering Committee. A response to these comments is provided
in Unit VI.
In the Federal Register of August 21, 2002 (67 FR 54196) (FRL-7190-
9), EPA issued a notice pursuant to section 408 of FFDCA, 21 U.S.C.
346a, as amended by FQPA (Public Law 104-170), announcing the filing of
a pesticide petition (PP 2E6404) by Interregional Research Project
Number 4 (IR-4), 681 US Highway 1 South, North Brunswick, NJ
08902-3390. That notice included a summary of the petition prepared by
IR-4, the petitioner. There were no comments received in response to
the notice of filing.
In the Federal Register of August 15, 2003 (68 FR 48908) (FRL-7322-
9), EPA issued a notice pursuant to section 408 of FFDCA, 21 U.S.C.
346a, as amended by FQPA (Public Law 104-170), announcing the filing of
amended pesticide petitions (PP 0F6140 and PP OF6210) by Bayer
CropScience, PO Box 12014, 2 T. W. Alexander Drive, Research Triangle
Park, NC 27709. That notice included a summary of the petition prepared
by Bayer CropScience. Two hundred and sixty five comments were filed. A
response to these comments is provided in Unit VI.
The petitions requested that 40 CFR 180.473(a)(1) be amended by
establishing tolerances for residues of the herbicide glufosinate
ammonium (butanoic acid, 2-amino-4-(hydroxymethylphosphinyl)-,
monoammonium salt) and its metabolite, 3-methylphosphinico-propionic
acid, expressed as 2-amino-4-(hydroxymethylphosphinyl)butanoic acid
equivalents in or on the raw agricultural commodities derived from
cotton, undelinted seed at 3.5 parts per million (ppm) and gin
byproducts at 12.0 ppm; and blueberry, lingonberry, juneberry and salal
at 0.10 ppm and that 40 CFR 180.473(a)(2) be amended by establishing
tolerances for residues of the herbicide glufosinate ammonium (butanoic
acid, 2-amino-4-(hydroxymethylphosphinyl)-, monoammonium salt) and its
metabolites, 3-methylphosphinico-propionic acid, and 2-acetamido-4-
methylphosphinico-butanoic acid expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents in or on the raw
agricultural commodities derived from transgenic cotton tolerant to
glufosinate ammonium: undelinted seed at 3.5 ppm and gin byproducts at
12.0 ppm and transgenic rice tolerant to glufosinate ammonium: grain at
1.0 ppm, straw at 1.6 ppm.
IR-4 and Bayer CropScience subsequently amended the petitions to
request that 40 CFR 180.473(a)(1) be amended by establishing tolerances
for residues of the herbicide glufosinate ammonium (butanoic acid, 2-
amino-4-(hydroxymethylphosphinyl)-, monoammonium salt) and its
metabolites, 2-acetamido-4-methylphosphinico-butanoic acid and 3-
methylphosphinico-propionic acid, expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents, in or on the
following food commodities: Bushberry subgroup, lingonberry, juneberry
and salal at 0.15 ppm, cattle, fat at 0.40 ppm, cattle, meat at 0.15
ppm, cattle, meat byproducts at 6.0 ppm, cotton, gin byproducts at 15
ppm, cotton, undelinted seed at 4.0 ppm, egg at 0.15 ppm, goat, fat at
0.40 ppm, goat, meat at 0.15 ppm, goat, meat byproducts at 6.0 ppm,
hog, fat at 0.40 ppm, hog, meat at 0.15 ppm, hog, meat byproducts at
6.0 ppm, horse, fat at 0.40 ppm, horse, meat at 0.15 ppm, horse, meat
byproducts at 6.0 ppm, Milk at 0.15 ppm, poultry, fat at 0.15 ppm,
poultry, meat at 0.15 ppm, poultry, meat byproducts 0.6 ppm, sheep, fat
at 0.40 ppm, sheep, meat at 0.15 ppm, and sheep, meat byproducts at 6.0
ppm.
Bayer CropScience subsequently amended the petitions to request
that 40 CFR 180.473(a)(2) be amended by establishing tolerances for
residues of the herbicide glufosinate ammonium (butanoic acid, 2-amino-
4-(hydroxymethylphosphinyl)-, monoammonium salt) and its metabolites,
2-acetamido-4-methylphosphinico-butanoic acid and 3-methylphosphinico-
propionic acid, expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents, in or on the
following raw agricultural and processed commodities derived from
transgenic cotton and rice that are tolerant to glufosinate ammonium:
Cotton, gin byproducts at 15 ppm, cotton, undelinted seed at 4.0 ppm,
rice, grain at 1.0 ppm, rice, straw at 2.0 ppm, and rice, hull at 2.0
ppm. These amendments were included in the August 15, 2003 notice of
filing.
Section 408(b)(2)(A)(i) of the FFDCA allows EPA to establish a
tolerance (the legal limit for a pesticide chemical residue in or on a
food) only if EPA determines that the tolerance is ``safe.'' Section
408(b)(2)(A)(ii) of the FFDCA defines ``safe'' to mean that ``there is
a reasonable certainty that no harm will result from aggregate exposure
to the pesticide chemical residue, including all anticipated dietary
exposures and all other exposures for which there is reliable
information.'' This includes exposure through drinking water and in
residential settings, but does not include occupational exposure.
Section 408(b)(2)(C) of the FFDCA requires EPA to give special
consideration to exposure of infants and children to the pesticide
chemical residue in establishing a tolerance and to ``ensure that there
is a reasonable certainty that no harm will result to infants and
children from aggregate exposure to the pesticide chemical
residue....''
EPA performs a number of analyses to determine the risks from
aggregate exposure to pesticide residues. For further discussion of the
regulatory requirements of section 408 of the FFDCA and a complete
description of the risk assessment process, see the final rule on
Bifenthrin Pesticide Tolerances (62 FR 62961, November 26, 1997) (FRL-
5754-7).
III. Aggregate Risk Assessment and Determination of Safety
Consistent with section 408(b)(2)(D) of the FFDCA, EPA has reviewed
the available scientific data and other relevant information in support
of this action. EPA has sufficient data to assess the hazards of and to
make a determination on aggregate exposure, consistent with section
408(b)(2) of the FFDCA, for a tolerance for combined residues of
glufosinate ammonium and its metabolites on bushberry subgroup,
lingonberry, juneberry and salal at 0.15 ppm, cattle, fat at 0.40 ppm,
cattle, meat at 0.15 ppm, cattle, meat byproducts at 6.0 ppm, cotton,
gin byproducts at 15 ppm, cotton, undelinted seed at 4.0 ppm, egg at
0.15 ppm, goat, fat at 0.40 ppm, goat, meat at 0.15 ppm, goat, meat
byproducts at 6.0 ppm, hog, fat at 0.40 ppm, hog, meat at 0.15 ppm,
hog, meat byproducts at 6.0 ppm, horse, fat at 0.40 ppm, horse, meat at
0.15 ppm, horse, meat byproducts at 6.0 ppm, milk at 0.15 ppm, poultry,
fat at 0.15 ppm, poultry, meat at 0.15 ppm, poultry, meat byproducts at
0.60 ppm, sheep, fat at 0.40 ppm, sheep, meat at 0.15 ppm, and sheep,
meat byproducts at 6.0 ppm, cotton, gin byproducts at 15 ppm, rice,
grain at 1.0 ppm, rice, straw at 2.0 ppm, and rice, hull at 2.0 ppm.
EPA's assessment of exposures and risks associated with establishing
the tolerance follows.
A. Toxicological Profile
EPA has evaluated the available toxicity data and considered its
validity, completeness, and reliability as well as the relationship of
the results of the studies to human risk. EPA has also considered
available information concerning the variability of the sensitivities
of major identifiable subgroups of consumers, including infants and
children. The nature of the
[[Page 55835]]
toxic effects caused by glufosinate ammonium and its metabolites are
discussed in Tables 1, 2 and 3 of this unit as well as the no-observed-
adverse-effect-level (NOAEL) and the lowest-observed-adverse-effect-
level (LOAEL) from the toxicity studies reviewed.
Table 1.--Glufosiante-ammonium: Acute, Subchronic, Chronic, and Other
Toxicity
------------------------------------------------------------------------
Guideline No. Study Type Results
------------------------------------------------------------------------
81-1 Acute oral LD50 = 4,010 mg/kg
(milligram/kilogram)
in males
LD50 = 3,030 mg/kg in
females
------------------------------------------------------------------------
870.3100 90-Day oral NOAEL = 6.2-8.8 mg/kg/
toxicity in rats day in males
(males only) LOAEL = 64-90 mg/kg/
day in males, based
on glutamine
synthetase
inhibition in the
brains
------------------------------------------------------------------------
870.3100 N-acetyl-L- NOAEL = 65-90 mg/kg/
glufosinate day in males
disodium LOAEL = 657-935 mg/kg/
90-Day oral day in males, based
toxicity in rats on glutamine
(males only). synthetase
inhibition in the
brains
------------------------------------------------------------------------
870.3100 90-Day oral NOAEL = 48 mg/kg/day
toxicity in in males, 192 mg/kg/
mouse day in females
Highest Dose Tested
(HDT)
LOAEL = 192 mg/kg/day
in males based on
the changes in
clinical
biochemistry and
liver weights in
males
------------------------------------------------------------------------
870.3200 21/28-Day dermal NOAEL = 100 mg/kg/day
toxicity in rat LOAEL = 300 mg/kg/day
based on clinical
observations
(aggressive
behavior,
piloerection, and a
high startle
response)
------------------------------------------------------------------------
870.3700 Prenatal Maternal: NOAEL = 10
developmental in mg/kg/day
rats (three LOAEL = 50 mg/kg/day
studies based on vaginal
combined) bleeding and
hyperactivity
Developmental: NOAEL
= 50 mg/kg/day
LOAEL =250 mg/kg/day
based on dilated
renal pelvis
------------------------------------------------------------------------
870.3700 Prenatal Maternal: NOAEL = 6.3
developmental in mg/kg/day
rabbit LOAEL = 20.0 mg/kg/
day based on reduced
food consumption,
body weight and
weight gains
Developmental: NOAEL
= 6.3 mg/kg/day
LOAEL = 20.0 based on
decreased body
weights and fetal
death
------------------------------------------------------------------------
870.3800 Reproduction and Parental/Systemic
fertility NOAEL = 18.0 mg/kg/
effects in rat day (HDT)
LOAEL = not
established
Reproductive NOAEL =
6.0 mg/kg/day
LOAEL = 18.0 mg/kg/
day based on
decreased number of
viable pups
Offspring NOAEL = 6.0
mg/kg/day
LOAEL = 18.0 mg/kg/
day based on
decreased number of
viable pups
------------------------------------------------------------------------
870.4100 Chronic toxicity NOAEL = 5.0 mg/kg/day
in dogs LOAEL = 8.5 mg/kg/day
based on mortality
(week 2) and
alterations in the
electrocardiogram at
6 months
------------------------------------------------------------------------
870.4200 Carcinogenicity NOAEL = 45.4 mg/kg/
in rats day in males, 57.1
mg/kg/day in females
LOAEL = 228.9 mg/kg/
day in males and
281.5 based on
increased incidences
of retinal atrophy.
No evidence of
carcinogenicity
------------------------------------------------------------------------
870.4300 Chronic Feeding / NOAEL = 24.4 mg/kg/
Carcinogenicity day in males, 8.2 mg/
in rats kg/day in females
LOAEL = not achieved
in males and 28.7
based on inhibition
of brain glutamate
synthetase in
females at 130 weeks
No evidence of
carcinogenicity
------------------------------------------------------------------------
870.4300 Carcinogenicity NOAEL = 10.82 mg/kg/
mice day in males, 16.19
mg/kg/day in females
LOAEL = 22.60 mg/kg/
day in males, 63.96
mg/kg/day in females
based on increased
mortality and
glucose levels and
consistent changes
in glutathione
levels in males,
increased glucose
levels and decreased
albumin and total
proteins
No evidence of
carcinogenicity
------------------------------------------------------------------------
870.5265 Reverse Mutation Glufosinate ammonium
Assay failed to cause
reverse mutations in
bacteria with and
without metabolic
activation.
------------------------------------------------------------------------
870.5300 Detection of gene Glufosinate ammonium
mutations in did not increase the
somatic cells in mutation frequency
culture at the thymidine
kinase locus
------------------------------------------------------------------------
870.5395 In vivo mammalian The results indicated
cytogenetic glufosinate ammonium
tests had no effect on
micronucleus
formation
------------------------------------------------------------------------
[[Page 55836]]
870.5500 Bacterial DNA glufosinate ammonium
damage or repair failed to cause
test damage to DNA that
could be detected by
this repair assay
------------------------------------------------------------------------
870.5550 Unscheduled DNA There was no evidence
synthesis in that unscheduled DNA
mammalian cells synthesis was
in culture induced by
glufosinate
ammonium.
------------------------------------------------------------------------
870.6200 Acute NOAEL = 500 mg/kg in
neurotoxicity in males and females
rat (2 studies) (HDT)
LOAEL = Not
established in both
sexes
------------------------------------------------------------------------
870.6200 Repeat Dose NOAEL = 1.5 mg/kg/day
Neurotoxicity in in males, 1.8 mg/kg/
rat day in females
LOAEL = 14.9 mg/kg/
day in males, 17.1
mg/kg/day in
females, based on
the inhibition of
glutamate synthetase
in the brain
------------------------------------------------------------------------
870.7485 Metabolism and The majority of the
pharmacokinetics radioactivity (95-
in rat 98% of the dose) was
eliminated during
the first 24 hrs
after dosing. The
parent compound,
glufosinate
ammonium, accounted
for most of the
eliminated
radioactivity in the
urine and feces of
both males (80% of
the dose) and
females (73% of the
dose). The
metabolite, 3-
methylphosphinico-
propionic acid, was
consistently found
in both urine and
feces of both sexes.
------------------------------------------------------------------------
870.7485 Metabolism and The majority of the
pharmacokinetics radioactivity was
in rat eliminated during
the first 24 to 48
hrs after dosing.
The parent compound,
glufosinate
ammonium, accounted
for the majority of
the radioactivity
eliminated in the
excreta of both
males ([]80% of
the dose) and
females (88% of the
dose). The
metabolite, 3-
methylphosphinico-
propionic acid, was
consistently found
in both urine (0.22-
1.20% of the dose)
and feces (0.44-
1.36% of the dose)
of both sexes. 2-
acetamido-4-
methylphosphinico-
butanoic acid was
found in feces (0.28-
1.72% of the dose)
of both male and
female rats and
barely above or at
the level of the
detection in the
urine of both sexes
(0.02-0.04% of the
dose). Very little
if any of
administered
glufosinate ammonium
was sequestered in
any tissues
examined.
------------------------------------------------------------------------
870.7485 Metabolism and The major route of
pharmacokinetics excretion was via
in rat feces (88% and 84%
of the administered
radioactivity for
males and females,
respectively).
Within 7 days of
post dosing, greater
than 94% of the dose
was eliminated.
Kinetics analysis
indicated that the
process of excretion
was a two-phase
process. The tissue
radioactivity level
for kidneys, liver
and gonads was just
above the background
level.
------------------------------------------------------------------------
870.7485 Metabolism and The majority of the
pharmacokinetics radioactivity was
in rat excreted within 24
hrs after the last
dose. The major
route of elimination
was via feces. There
was also a two-
phased elimination
process. More
radioactivity was
found in the tissues
of animals dosed
repeatedly than that
of animals receiving
a single dose.
------------------------------------------------------------------------
870.7600 Dermal The results indicate
penetration that at the low dose
(0.1 mg) 42.5 to
50.8% of the applied
radioactivity was
absorbed whereas at
the high dose (10
mg) 26% was
absorbed. After
removal and washing
of the treated skin
a substantial amount
of the radioactivity
still remained in
the skin, and it was
gradually absorbed
and eliminated.
Radioactivity was
found in both feces
and urine samples,
but the majority of
glufosinate ammonium
was eliminated in
the urine. In all
organs/tissues
examined,
radioactivity was
found to reach a
maximum level either
at 4 or 10 hrs after
exposure.
Subsequently, the
radioactivity
dropped rapidly. The
amount of
radioactivity found
in the brain was
very minimal
relative to that of
kidneys and liver.
------------------------------------------------------------------------
Table 2.--3-Methylphosphinico-propionic Acid: Subchronic Toxicity
------------------------------------------------------------------------
Guideline No. Study Type Results
------------------------------------------------------------------------
870.3100 90-Day dermal NOAEL = 102 mg/kg/
toxicity in rats day in males, 113
mg/kg/day in
females
LOAEL = 420 mg/kg/
day in males, 439
mg/kg/day in
females based on
increased
reticulocytes and
increased
absolute and
relative liver
weights in males
------------------------------------------------------------------------
870.3100 90-Day dermal NOAEL = 1,121 mg/
toxicity in mice kg/day in males,
1,340 mg/kg/day
in females
LOAEL = Not
established
------------------------------------------------------------------------
[[Page 55837]]
870.3700 Prenatal Maternal: NOAEL =
developmental in 300 mg/kg/day
rodents in rats Maternal: LOAEL =
900 mg/kg/day
based on one
death and
clinical findings
(persistent
piloerection and/
or increased
urinary output)
Developmental:
NOAEL = 300 mg/kg/
day
Developmental:
LOAEL = 900 mg/kg/
day based on
increases in the
incidences of
total litter loss
and in the fetal
and litter
incidences of
wavy and/or
thickened ribs.
------------------------------------------------------------------------
870.3700 Prenatal Maternal: NOAEL =
developmental in 50 mg/kg/day
rabbits Maternal: LOAEL =
100 mg/kg/day
based on
increased
abortions,
mortality, and
reductions in
food and water
consumption, body
weight gain, and
fecal output
Developmental:
NOAEL = 200 mg/kg/
day
Developmental:
LOAEL = Not
observed
------------------------------------------------------------------------
Table 3.--Metabolite, 2-acetomido-4-methylphosphinico-butanoic:
Subchronic and Other Toxicity
------------------------------------------------------------------------
Guideline No. Study Type Results
------------------------------------------------------------------------
870.3100 90-Day oral NOAEL = 147 mg/kg/day
toxicity rodents in males, 162 mg/kg/
in rats day in females
LOAEL = 738 mg/kg/day
in males, 800 mg/kg/
day in females based
on glutamine
synthetase
inhibition in the
brain
------------------------------------------------------------------------
870.3100 90-Day oral NOAEL = Not
toxicity rodents established for
in mice males, 110 mg/kg/day
in females
LOAEL = 83 mg/kg/day
in males, 436 mg/kg/
day in females based
on glutamine
synthetase
inhibition in the
brain
------------------------------------------------------------------------
870.3150 Subchronic NOAEL = 19 mg/kg/day
Nonrodent Oral in males, 21 mg/kg/
Toxicity in dogs day in females
LOAEL = 72 mg/kg/day
in males, 79 mg/kg/
day in females based
on glutamine
synthetase
inhibition in the
brain
------------------------------------------------------------------------
870.3700 Prenatal Maternal: NOAEL =
developmental in 1,000 mg/kg/day
rodents-rat Maternal: LOAEL = Not
observed
Developmental: NOAEL
= 1,000 mg/kg/day
Developmental: LOAEL
= Not observed
------------------------------------------------------------------------
870.3700 Prenatal Maternal: NOAEL = 64
developmental in mg/kg/day
rabbits Maternal: LOAEL = 160
mg/kg/day based on
reduced feed
consumption
Developmental: NOAEL
= 64 mg/kg/day
Developmental: LOAEL
= 160 based on uni-
or bilateral extra
at the 13th thoracic
vertebra
------------------------------------------------------------------------
870.6200 Acute NOAEL = 1,000 mg/kg
Neurotoxicity in in males and females
rats LOAEL = 2,000 mg/kg
in males and females
based on clinical
signs of toxicity
including sedation,
ruffled fur, and
diarrhea
------------------------------------------------------------------------
870.6200 Acute NOAEL = 100 mg/kg in
Neurotoxicity in males and females
rats LOAEL = 1,000 mg/kg
in males and females
based on decreased
body weight gain
------------------------------------------------------------------------
870.6200 Repeat Dose NOAEL = 158.9 mg/kg/
Neurotoxicity in day in males, 179.4
rats mg/kg/day in females
LOAEL = Not
established in males
and females
------------------------------------------------------------------------
B. Toxicological Endpoints
The dose at which no adverse effects are observed (the NOAEL) from
the toxicology study identified as appropriate for use in risk
assessment is used to estimate the toxicological level of concern
(LOC). However, the lowest dose at which adverse effects of concern are
identified (the LOAEL) is sometimes used for risk assessment if no
NOAEL was achieved in the toxicology study selected. An uncertainty
factor (UF) is applied to reflect uncertainties inherent in the
extrapolation from laboratory animal data to humans and in the
variations in sensitivity among members of the human population as well
as other unknowns. An UF of 100 is routinely used, 10X to account for
interspecies differences and 10X for intraspecies differences. A 10x
data base uncertainty factor, due to the lack of a developmental
neurotoxicity study, was applied to all dietary and residential dermal,
inhalation, and incidental oral exposure assessments. For residential
inhalation exposure assessments an additional 10x data base uncertainty
factor was applied due to the lack of an adequate inhalation study and
high concern for exposure via the inhalation route (10,000). Agency
policy limits the total uncertainty factor applied for any particular
chemical to no more than 3,000 (see EPA report ``A Review of the
Reference Dose and Reference Concentration Processes:'' EPA/630/P-02/
022F, December 2002; a Notice of Availability of the Final Report was
published in the Federal Register of
[[Page 55838]]
May 21, 2003 (68 FR 27805) (FRL-7501-8).
For dietary risk assessment (other than cancer) the Agency uses the
UF to calculate an acute or chronic reference dose (acute RfD or
chronic RfD) where the RfD is equal to the NOAEL divided by the
appropriate UF (RfD = NOAEL/UF). Where an additional safety factors
(SF) is retained due to concerns unique to the FQPA, this additional
factor is applied to the RfD by dividing the RfD by such additional
factor. The acute or chronic Population Adjusted Dose (aPAD or cPAD) is
a modification of the RfD to accommodate this type of FQPA SF.
For non-dietary risk assessments (other than cancer) the UF is used
to determine the LOC. For example, when 100 is the appropriate UF (10X
to account for interspecies differences and 10X for intraspecies
differences) the LOC is 100. To estimate risk, a ratio of the NOAEL to
exposures (margin of exposure (MOE) = NOAEL/exposure) is calculated and
compared to the LOC.
The linear default risk methodology (Q*) is the primary method
currently used by the Agency to quantify carcinogenic risk. The Q*
approach assumes that any amount of exposure will lead to some degree
of cancer risk. A Q* is calculated and used to estimate risk which
represents a probability of occurrence of additional cancer cases
(e.g., risk is expressed as 1 x 10-6 or one in a million).
Under certain specific circumstances, MOE calculations will be used for
the carcinogenic risk assessment. In this non-linear approach, a
``point of departure'' is identified below which carcinogenic effects
are not expected. The point of departure is typically a NOAEL based on
an endpoint related to cancer effects though it may be a different
value derived from the dose response curve. To estimate risk, a ratio
of the point of departure to exposure (MOEcancer = point of
departure/exposures) is calculated. A summary of the toxicological
endpoints for glufosinate ammonium and its metabolite used for human
risk assessment is shown in Table 4 of this unit:
Table 4.--Summary of Toxicological Dose and Endpoints for Glufosinate ammonium and its Metabolites for Use in
Human Risk Assessment
----------------------------------------------------------------------------------------------------------------
FQPA SF* and Level of
Exposure Scenario Dose Used in Risk Concern for Risk Study and Toxicological
Assessment, UF Assessment Effects
----------------------------------------------------------------------------------------------------------------
Acute Dietary (Females 13-50 years of NOAEL = 6.3 mg/kg/day FQPA SF = 1 Prenatal Developmental
age) UF = 1,000............. aPAD = acute RfD / FQPA Toxicity Study in non-
Acute RfD = 0.0063 mg/ SF = 0.0063 mg/kg/day. rodents - rabbit
kg/day. LOAEL = 20.0 mg/kg/day
based on decreased
body weights and fetal
death
-----------------------------------------------------------------------------------------
Chronic Dietary (All populations) NOAEL = 6.0 mg/kg/day FQPA SF = 1 cPAD = ``Weight-of-evidence''
UF = 1,000............. chronic RfD / FQPA SF approach from several
Chronic RfD = 0.006 mg/ = 0.006 mg/kg/day studies; NOAEL = 6.0
kg/day. mg/kg/day; brain
glutamine synthetase
inhibition and
alterations in the
electrocardiogram.
-----------------------------------------------------------------------------------------
Short-Term Dermal (1 to 30 days) Oral study NOAEL = 6.3 LOC for MOE = 1,000 Prenatal Developmental
(Residential) mg/kg/day (dermal (Residential) Toxicity Study in non-
absorption rate = 50%) rodents - rabbits
LOAEL = 20 mg/kg/day
based on reduced fetal
body weights,
increased fetal
mortality, reduced
food consumption, body
weight, and body
weight gain
-----------------------------------------------------------------------------------------
Short-Term Inhalation (1 to 30 days) Oral study NOAEL = 6.3 LOC for MOE = 3,000 Prenatal Developmental
(Residential) mg/kg/day (inhalation (Residential) Toxicity Study in non-
absorption rate = rodents - rabbits
100%) LOAEL = 20 mg/kg/day
based on reduced fetal
body weights,
increased fetal
mortality, reduced
food consumption, body
weight, and body
weight gain
----------------------------------------------------------------------------------------------------------------
*The reference to the FQPA SF refers to any additional SF retained due to concerns unique to the FQPA.
C. Exposure Assessment
1. Dietary exposure from food and feed uses. Tolerances have been
established (40 CFR 180.473) for the combined residues of glufosinate
ammonium and its metabolites, in or on almond hulls, apples, bananas,
meat, milk, fat, meat byproducts, eggs, grapes, potatoes, tree nuts and
food commodities derived from transgenic canola, transgenic field corn,
transgenic soybean and transgenic sugar beets. Risk assessments were
conducted by EPA to assess dietary exposures from combined residues of
glufosinate ammonium and its metabolites as follows:
i. Acute exposure. Acute dietary risk assessments are performed for
a food-use pesticide if a toxicological study has indicated the
possibility of an effect of concern occurring as a result of a one day
or single exposure. The Dietary Exposure Evaluation Model-Food
Consumption Intake Database (DEEM-FCID[reg]) analysis
evaluated the individual food consumption as reported by respondents in
the USDA 1994-1996 and 1998 nationwide Continuing Surveys of Food
Intake by Individuals (CSFII) and accumulated exposure to the chemical
for each commodity. The following assumptions were made for the acute
exposure assessments: 100% crop treated for all registered and proposed
commodities (Tier 1 analysis) and, depending on the level of blending
of a commodity, tolerance level residues, highest field trial, or
average field trial.
ii. Chronic exposure. In conducting this chronic dietary risk
assessment the DEEM-FCID[reg] analysis evaluated the
individual food consumption as reported by respondents in the USDA
1994-1996 and 1998 nationwide CSFII and accumulated exposure to the
chemical for each commodity. The following assumptions were made for
the chronic exposure assessments: 100% crop treated for all registered
and proposed commodities (Tier 1 analysis) excluding apple, canola,
corn and grape, where 3 year weighted average percent crop treated was
used, and, depending
[[Page 55839]]
on the level of blending of a commodity, tolerance level residues or
average field trial.
iii. Cancer. No evidence of carcinogenicity at doses tested were
observed in the mouse and rat carcinogenicity studies. A quantitative
cancer risk assessment was not performed for glufosinate ammonium.
iv. Anticipated residue and percent crop treated (PCT) information.
Section 408(b)(2)(F) of the FFDCA states that the Agency may use data
on the actual percent of food treated for assessing chronic dietary
risk only if the Agency can make the following findings: Condition 1,
that the data used are reliable and provide a valid basis to show what
percentage of the food derived from such crop is likely to contain such
pesticide residue; Condition 2, that the exposure estimate does not
underestimate exposure for any significant subpopulation group; and
Condition 3, if data are available on pesticide use and food
consumption in a particular area, the exposure estimate does not
understate exposure for the population in such area. In addition, the
Agency must provide for periodic evaluation of any estimates used. To
provide for the periodic evaluation of the estimate of PCT as required
by section 408(b)(2)(F) of the FFDCA, EPA may require registrants to
submit data on PCT.
The Agency believes that the three conditions listed in Unit IV.
have been met. With respect to Condition 1, PCT estimates are derived
from Federal and private market survey data, which are reliable and
have a valid basis. EPA uses a weighted average PCT for chronic dietary
exposure estimates. This weighted average PCT figure is derived by
averaging State-level data for a period of up to 3 years, and weighting
for the more robust and recent data. A weighted average of the PCT
reasonably represents a person's dietary exposure over a lifetime, and
is unlikely to underestimate exposure to an individual because of the
fact that pesticide use patterns (both regionally and nationally) tend
to change continuously over time, such that an individual is unlikely
to be exposed to more than the average PCT over a lifetime. For acute
dietary exposure estimates, EPA uses an estimated maximum PCT. The
exposure estimates resulting from this approach reasonably represent
the highest levels to which an individual could be exposed, and are
unlikely to underestimate an individual's acute dietary exposure. The
Agency is reasonably certain that the percentage of the food treated is
not likely to be an underestimation. As to Conditions 2 and 3, regional
consumption information and consumption information for significant
subpopulations is taken into account through EPA's computer-based model
for evaluating the exposure of significant subpopulations, including
several regional groups. Use of this consumption information in EPA's
risk assessment process ensures that EPA's exposure estimate does not
understate exposure for any significant subpopulation group and allows
the Agency to be reasonably certain that no regional population is
exposed to residue levels higher than those estimated by the Agency.
Other than the data available through national food consumption
surveys, EPA does not have available information on the regional
consumption of food to which glufosinate ammonium may be applied in a
particular area.
2. Dietary exposure from drinking water. The Agency lacks
sufficient monitoring exposure data to complete a comprehensive dietary
exposure analysis and risk assessment for glufosinate ammonium in
drinking water. Because the Agency does not have comprehensive
monitoring data, drinking water concentration estimates are made by
reliance on simulation or modeling taking into account data on the
physical characteristics of glufosinate ammonium. Based on
environmental fate data the residues of concern in drinking water are
glufosinate ammonium, 3-methylphosphinico-propionic acid, 2-
methylphosphinico-acetic acid and N-acetyl-glufosinate.
The Agency uses the First Index Reservoir Screening Tool (FIRST) or
the Pesticide Root Zone/Exposure Analysis Modeling System (PRZM/EXAMS),
to produce estimates of pesticide concentrations in an index reservoir.
The SCI-GROW model is used to predict pesticide concentrations in
shallow groundwater. For a screening-level assessment for surface water
EPA will use FIRST (a tier 1 model) before using PRZM/EXAMS (a tier 2
model). The FIRST model is a subset of the PRZM/EXAMS model that uses a
specific high-end runoff scenario for pesticides. While both FIRST and
PRZM/EXAMS incorporate an index reservoir environment, the PRZM/EXAMS
model includes a percent crop area factor as an adjustment to account
for the maximum percent crop coverage within a watershed or drainage
basin.
None of these models include consideration of the impact processing
(mixing, dilution, or treatment) of raw water for distribution as
drinking water would likely have on the removal of pesticides from the
source water. The primary use of these models by the Agency at this
stage is to provide a coarse screen for sorting out pesticides for
which it is highly unlikely that drinking water concentrations would
ever exceed human health levels of concern.
Since the models used are considered to be screening tools in the
risk assessment process, the Agency does not use estimated
environmental concentrations (EECs) from these models to quantify
drinking water exposure and risk as a %RfD or %PAD. Instead, drinking
water levels of comparison (DWLOCs) are calculated and used as a point
of comparison against the model estimates of a pesticide's
concentration in water. DWLOCs are theoretical upper limits on a
pesticide's concentration in drinking water in light of total aggregate
exposure to a pesticide in food, and from residential uses. Since
DWLOCs address total aggregate exposure to glufosinate ammonium they
are further discussed in the aggregate risk sections in Unit III.E.
Based on the PRZM-EXAMS and SCI-GROW models the EECs of glufosinate
ammonium and its degradates for acute exposures are estimated to be 94
[mu]g/liter for surface water and 9 [mu]g/liter for ground water. The
EECs for chronic exposures are estimated to be 43 [mu]g/liter for
surface water and 9 [mu]g/liter for ground water.
3. The term ``residential exposure'' is used in this document to
refer to non-occupational, non-dietary exposure (e.g., for lawn and
garden pest control, indoor pest control, termiticides, and flea and
tick control on pets).
Glufosinate ammonium is currently registered for use on the
following residential non-dietary sites: Home use for spot treatment of
weeds, grass, bushes and vines. The risk assessment was conducted using
the following residential exposure assumptions: Application rate of
0.0312 lb active ingredient (ai) per 1,000 ft2, dermal unit
exposure of 11 mg/lb and inhalation exposure of 0.016 mg/lb from hose
end application and dermal unit exposure of 56 mg/lb and inhalation
exposure of 0.0065 mg/lb from low pressure hand wand application.
4. Cumulative exposure to substances with a common mechanism of
toxicity. Section 408(b)(2)(D)(v) of the FFDCA requires that, when
considering whether to establish, modify, or revoke a tolerance, the
Agency consider ``available information'' concerning the cumulative
effects of a particular pesticide's residues and ``other substances
that have a common mechanism of toxicity.''
[[Page 55840]]
EPA does not have, at this time, available data to determine
whether glufosinate ammonium has a common mechanism of toxicity with
other substances. Unlike other pesticides for which EPA has followed a
cumulative risk approach based on a common mechanism of toxicity, EPA
has not made a common mechanism of toxicity finding for glufosinate
ammonium and any other substances and glufosinate ammonium does not
appear to produce a toxic metabolite produced by other substances. For
the purposes of this tolerance action; therefore, EPA has not assumed
that glufosinate ammonium has a common mechanism of toxicity with other
substances. For information regarding EPA's efforts to determine which
chemicals have a common mechanism of toxicity and to evaluate the
cumulative effects of such chemicals, see the policy statements
released by EPA's Office of Pesticide Programs concerning common
mechanism determinations and procedures for cumulating effects from
substances found to have a common mechanism on EPA's website at http://www.epa.gov/pesticides/cumulative/
.
D. Safety Factor for Infants and Children
1. In general. Section 408 of the FFDCA provides that EPA shall
apply an additional tenfold margin of safety for infants and children
in the case of threshold effects to account for prenatal and postnatal
toxicity and the completeness of the data base on toxicity and exposure
unless EPA determines that a different margin of safety will be safe
for infants and children. Margins of safety are incorporated into EPA
risk assessments either directly through use of a MOE analysis or
through using uncertainty (safety) factors in calculating a dose level
that poses no appreciable risk to humans.
2. Prenatal and postnatal sensitivity. The studies examining
prenatal and postnatal toxicity showed:
a. No quantitative or qualitative evidence of increased
susceptibility following in utero exposure in the prenatal
developmental study in rats.
b. Qualitative evidence of increased susceptibility in the prenatal
developmental study in rabbits and quantitative evidence of increased
susceptibility in the 2-generation reproduction study in rats. In this
study, a decrease in the number of viable pups was observed in the
absence of parental toxicity at any dose.
Since there is qualitative evidence of increased susceptibility of
the young following exposure to glufosinate ammonium, EPA performed a
degree of concern analysis to: Determine the level of concern for the
effects observed when considered in the context of all available
toxicity data; and identify any residual uncertainties after
establishing toxicity endpoints and traditional uncertainty factors to
be used in the risk assessment of this chemical. In the rabbit
developmental study the degree of concern observed as low noting that
the fetal effects of concern occurred only at the highest dose tested
and that a clear NOAEL for effects was established. In the 2-generation
reproduction study the degree of concern for the effects observed as
low noting that clear NOAELs and LOAELs were identified for the
offspring effects of concern and the dose-response well-characterized.
3. Conclusion. There is not an adequate toxicity data base for
glufosinate ammonium and its metabolites although the exposure data are
complete or are estimated based on data that reasonably account for
potential exposures. EPA identified the following data gaps:
a. Acute neurotoxicity study conducted in the rat which includes
glutamine synthetase activity measurement in the liver, kidneys, and
brain.
b. A developmental neurotoxicity (DNT) study conducted in the rat
which includes comparative glutamine synthetase activity measurement in
the liver, kidneys, and brain of the pups and mothers.
c. A 28-day inhalation toxicity study in rats with glutamine
synthetase activity measurements in brain, kidney, liver and lung.
EPA is also requesting additional data to confirm that liver and
kidney changes, observed in the absence of histopathological changes,
are an adaptive response and not an adverse effect. These studies are
required because the glutamine synthetase measurements are not
available in young and adult animals. Therefore, EPA has applied
additional data base uncertainty factors in this risk assessment. The
results of these studies are expected to eliminate any uncertainty that
may be associated in characterizing the toxicity of glufosinate
ammonium.
For dietary risk assessment, an FQPA additional 10X safety factor,
retained as a data base uncertainty factor due to the lack of a
developmental neurotoxicity (DNT) study that measures glutamine
synthetase activity in the young and adult animals, was applied to all
dietary and residential dermal, inhalation, and incidental oral
exposure assessments. For residential inhalation exposure assessments
an additional 10x data base uncertainty factor was applied due to the
lack of an adequate inhalation study and high concern for exposure via
the inhalation route with a total uncertainty factor of 3,000 applied
based on EPA policy cited in Unit III.B.
E. Aggregate Risks and Determination of Safety
To estimate total aggregate exposure to a pesticide from food,
drinking water, and residential uses, the Agency calculates DWLOCs
which are used as a point of comparison against the model estimates of
a pesticide's concentration in water (EECs). DWLOC values are not
regulatory standards for drinking water. DWLOCs are theoretical upper
limits on a pesticide's concentration in drinking water in light of
total aggregate exposure to a pesticide in food and residential uses.
In calculating a DWLOC, the Agency determines how much of the
acceptable exposure (i.e., the PAD) is available for exposure through
drinking water [e.g., allowable chronic water exposure (mg/kg/day) =
cPAD - (average food + residential exposure)]. This allowable exposure
through drinking water is used to calculate a DWLOC.
A DWLOC will vary depending on the toxic endpoint, drinking water
consumption, and body weights. Default body weights and consumption
values as used by the USEPA Office of Water are used to calculate
DWLOCs: 2 liter (L)/70 kg (adult male), 2L/60 kg (adult female), and
1L/10 kg (child). Default body weights and drinking water consumption
values vary on an individual basis. This variation will be taken into
account in more refined screening-level and quantitative drinking water
exposure assessments. Different populations will have different DWLOCs.
Generally, a DWLOC is calculated for each type of risk assessment used:
Acute, short-term, intermediate-term, chronic, and cancer.
When EECs for surface water and groundwater are less than the
calculated DWLOCs, EPA concludes with reasonable certainty that
exposures to the pesticide in drinking water (when considered along
with other sources of exposure for which EPA has reliable data) would
not result in unacceptable levels of aggregate human health risk at
this time. Because EPA considers the aggregate risk resulting from
multiple exposure pathways associated with a pesticide's uses, levels
of comparison in drinking water may vary as those uses change. If new
uses are added in the future, EPA will reassess the potential impacts
of residues of the pesticide in drinking water as a part of the
aggregate risk assessment process.
[[Page 55841]]
1. Acute risk. Using the exposure assumptions discussed in this
unit for acute exposure, the acute dietary exposure from food to
glufosinate ammonium will occupy 48% of the aPAD for females 13 years
and older. In addition, there is potential for acute dietary exposure
to glufosinate ammonium in drinking water. After calculating DWLOCs and
comparing them to the EECs for surface water and groundwater, EPA does
not expect the aggregate exposure to exceed 100% of the aPAD, as shown
in Table 5 of this unit:
Table 5.--Aggregate Risk Assessment for Acute Exposure to Glufosinate ammonium
----------------------------------------------------------------------------------------------------------------
Surface Ground Acute
aPAD (mg/ % aPAD Water EEC Water EEC DWLOC
Population Subgroup kg) (Food) ([mu]g/ ([mu]g/ ([mu]g/
liter) liter) liter)
----------------------------------------------------------------------------------------------------------------
Females (13-50 years old) 0.0063 48 94 9 98
----------------------------------------------------------------------------------------------------------------
2. Chronic risk. Using the exposure assumptions described in this
unit for chronic exposure, EPA has concluded that exposure to
glufosinate ammonium from food will utilize 10% of the cPAD for the
U.S. population, 20% of the cPAD for all infants and 27% of the cPAD
for children (1-2 years old). Based on the use pattern, chronic
residential exposure to residues of glufosinate ammonium is not
expected. In addition, there is potential for chronic dietary exposure
to glufosinate ammonium in drinking water. After calculating DWLOCs and
comparing them to the EECs for surface water and groundwater, EPA does
not expect the aggregate exposure to exceed 100% of the cPAD, as shown
in Table 6 of this unit:
Table 6.--Aggregate Risk Assessment for Chronic (Non-Cancer) Exposure to Glufosinate ammonium
----------------------------------------------------------------------------------------------------------------
Surface Ground Chronic
cPAD mg/kg/ % cPAD Water EEC Water EEC DWLOC
Population Subgroup day (Food) ([mu]g/ ([mu]g/ ([mu]g/
liter) liter) liter)
----------------------------------------------------------------------------------------------------------------
U.S. Population 0.006 10 43 9 189
----------------------------------------------------------------------------------------------------------------
Youth (13-19 years old) 0.006 9 43 9 164
----------------------------------------------------------------------------------------------------------------
Females (13-50 years old) 0.006 7 43 9 167
----------------------------------------------------------------------------------------------------------------
Adults (20-49) 0.006 8 43 9 194
----------------------------------------------------------------------------------------------------------------
3. Short-term risk. Short-term aggregate exposure takes into
account residential exposure plus chronic exposure to food and water
(considered to be a background exposure level).
Glufosinate ammonium is currently registered for use that could
result in short-term residential exposure and the Agency has determined
that it is appropriate to aggregate chronic food and water and short-
term exposures.
Using the exposure assumptions described in this unit for short-
term exposures, EPA has concluded that food and residential exposures
aggregated result in aggregate risk index (ARI) of 5.42 for the U.S.
population, 6.35 for females (13-49 years old) and 5.75 for youth (13-
19 years old). The registered spot treatment of weeds is expected to
result in residential exposure only to adults. Therefore, short-term
aggregate assessments were not conducted for infants and children.
These aggregate ARIs do not exceed the Agency's level of concern of
less than 1 for aggregate exposure to food and residential uses. In
addition, short-term DWLOCs were calculated and compared to the EECs
for chronic exposure of glufosinate ammonium in groundwater and surface
water. After calculating DWLOCs and comparing them to the EECs for
surface and ground water, EPA does not expect short-term aggregate
exposure to exceed the Agency's level of concern, as shown in Table 7
of this unit:
Table 7.--Aggregate Risk Assessment for Short-Term Exposure to Glufosinate ammonium
----------------------------------------------------------------------------------------------------------------
Aggregate
ARI\1\ (Food Surface Ground Short-Term
Population Subgroup + Water EEC Water EEC DWLOC (ppb)
Residential) (ppb) (ppb)
----------------------------------------------------------------------------------------------------------------
U.S. Population 5.42 43 9 180
----------------------------------------------------------------------------------------------------------------
Females (13-49 years old) 6.35 43 9 159
----------------------------------------------------------------------------------------------------------------
Youths (13-19 years old) 5.75 43 9 156
----------------------------------------------------------------------------------------------------------------
\1\ ARI = MOEcalculated ( i.e., food, dermal, inhalation) / MOEacceptable
4. Aggregate cancer risk for U.S. population. No evidence of
carcinogenicity at doses tested were observed in the mouse and rat
carcinogenicity studies. Therefore, no cancer risk is expected.
5. Determination of safety. Based on these risk assessments, EPA
concludes that there is a reasonable certainty that no harm will result
to the general population, and to infants and children from aggregate
exposure to glufosinate ammonium residues.
[[Page 55842]]
IV. Other Considerations
A. Analytical Enforcement Methodology
Adequate enforcement methodology (example--gas chromatography) is
available to enforce the tolerance expression. The method may be
requested from: Chief, Analytical Chemistry Branch, Environmental
Science Center, 701 Mapes Rd., Ft. Meade, MD 20755-5350; telephone number: (410) 305-2905; e-mail address: residuemethods@epa.gov.
B. International Residue Limits
Codex and Mexico do not have maximum residue limits (MRLs) for
glufosinate ammonium and its metabolites for the proposed crops or
livestock commodities. Canada does not have MRLs for glufosinate
ammonium and its metabolites for the proposed crops, poultry
commodities or milk, but does have a MRL of 1 ppm for ruminant liver
and kidney.
V. Conclusion
Therefore, the tolerance is established for combined residues of
glufosinate ammonium and its metabolites in or on bushberry subgroup,
Lingonberry, juneberry and salal at 0.15 ppm, cattle, fat at 0.40 ppm,
cattle, meat at 0.15 ppm, cattle, meat byproducts at 6.0 ppm, cotton,
gin byproducts at 15 ppm, cotton, undelinted seed at 4.0 ppm, egg at
0.15 ppm, goat, fat at 0.40 ppm, goat, meat at 0.15 ppm, goat, meat
byproducts at 6.0 ppm, hog, fat at 0.40 ppm, hog, meat at 0.15 ppm,
hog, meat byproducts at 6.0 ppm, horse, fat at 0.40 ppm, horse, meat at
0.15 ppm, horse, meat byproducts 6.0 ppm, Milk at 0.15 ppm, poultry,
fat at 0.15 ppm, poultry, meat at 0.15 ppm, poultry, meat byproducts
0.60 ppm, sheep, fat at 0.40 ppm, sheep, meat at 0.15 ppm, and sheep,
meat byproducts 6.0 ppm, cotton, gin byproducts at 15 ppm, rice, grain
at 1.0 ppm, rice, straw at 2.0 ppm, and rice, hull at 2.0 ppm.
VI. Response to Comments
The overall thrust of the comments from the Sierra Club was that
``large quantities of glufosinate ammonium herbicide will be utilized
on transgenic rice crops in the United States and abroad . . . even
though the herbicide may have side effects on humans, farm animals and
beneficial insects.'' The testing of pesticides will often reveal that
a pesticide has the potential to create adverse effects in animals and/
or insects; those risks are addressed via registration under FIFRA. The
critical issue addressed by FFDCA is whether there is an adequate
margin of safety between the aggregate exposure level of humans to the
pesticide and the level that potentially may be harmful. As EPA
described in Unit III.E. above, EPA's risk assessment showed that an
adequate margin was available for EPA to conclude that there is a
reasonable certainty of no harm for the general population including
infants and children.
EPA has reprinted each of Sierra Club's more specific comments
below and responded to each individually.
1. Comment--plant metabolism of glufosinate. A concern is other
plant metabolites of glufosinate ammonium may occur in addition to the
two primary metabolites identified in the grain and straw, since the
two substances did not appear to account for 100% of the total
radioactive residues in the two plant tissues tested. While more than
80% appeared to be accounted for, Aventis needs to identify whether
additional metabolites were produced. The two primary metabolites
identified as being typical of plant metabolism in the grain at harvest
were 3-methylphosphinicopropionic acid, being--70% of the total
radioactive residues (TRR). Another residue in the grain was N-acetyl-
L-glufosinate (2-acetamido-4-methylphosphinicobutanoic acid), at about
11% of the TRR and parent at 5-6% of the TRR. In the straw, 3-
methylphosphinicopropionic acid was the major metabolite comprising
approximately 60% of the TRR. Lesser amounts of the parent (about 17%
of the TRR) and N-acetylglufosinate (10-13% of TRR) were found in the
straw fraction.
Agency response. The transgenic rice metabolism study was conducted
according to the regulatory guideline requirements (OPPTS 860.1500) and
conformed to EPA Good Laboratory Practice (GLP) Standards (the % TRR
figures given below are averages of four samples). The study indicated
that glufosinate ammonium, N-acetyl-glufosinate, and 3-MP accounted for
88% and 91% of the total radioactive residue (TRR) found in rice grain
and rice straw, respectively (grain and straw are the only rice raw
agricultural commodities (RACs)). The remainder of the radioactivity
was identified as 2-methylphosphinico-acetic acid (grain--1% TRR;
straw--2% TRR), several unknowns when combined accounted for 2% TRR
(rice grain) and 3% TRR (rice straw), and fiber bound residues (grain--
8% TRR; straw--5% TRR). The petitioner identified/characterized 99% and
101% of the TRR in rice grain and rice straw, respectively. In
previously submitted transgenic canola and non-transgenic apple, corn,
lettuce, soybeans, and wheat metabolism studies, the petitioner
demonstrated the incorporation of radioactivity into nature plant
constituents. On the basis of the transgenic rice metabolism study and
the previously submitted metabolism studies, EPA concluded that the
residue identification/characterization procedures performed were
adequate and the residues of concern in transgenic rice, for purposes
of tolerance enforcement and risk assessment, are glufosinate ammonium,
N-acetyl-glufosinate, and 3-methylphosphinico-propionic acid (3-MP).
2. Comment--analytical method. We ask EPA if any independent
sampling and gas chromatography analyses were conducted besides that
performed by Aventis and its contractors. We request that an
independent sampling and G.C. analysis program be carried out if
Aventis has not had a third party independent contractor, since we are
skeptical of Aventis' sampling data and analyses. We generally agree
that the enforcement analytical method of utilizing gas chromatography
appears to be acceptable for detecting and measuring levels of
glufosinate ammonium and metabolites with a general limit of
quantification of 0.05 ppm to allow detection of glufosinate residues
at or above the proposed tolerances. We wonder if glufosinate residues
might have been found between 0.01 ppm and 0.05 ppm, and that due to
its toxicity, EPA should have required a lower detectability limit be
utilized to demonstrate if glufosinate residues were missed below 0.05
ppm or 50 parts per billion (ppb) concentration down to 1 ppb.
Agency response. The rice magnitude of the residue study was
conducted according to the regulatory guideline requirements (OPPTS
860.1500) and conformed to EPA GLP Standards. The rice grain and straw
samples were analyzed using a method similar to that previously
validated by an independent laboratory and by the EPA. Based on these
validation procedures and the validation and concurrent recovery data
submitted with the transgenic rice field trials, EPA concluded that the
method was appropriate for data collection purposes.
EPA understands that residues below the level of quantification (<
LOQ) does not mean that residues are not present. The dietary analyses
assumed average field trial residues for rice commodities. When
calculating the average, half LOQ residues were assumed for residues <
LOQ. Therefore, the dietary risk assessment took into account the
possibility of residues between 0.01 and
[[Page 55843]]
0.05 ppm. For further information on EPA's rationale for assuming half
LOQ residues see ``Values to Non-Detectable/Non-Quantifiable Residues
in Human Health Food Exposure Assessments'' (faxed upon request;
telephone: (202) 401-0527; item: 6047).
3. Comment--magnitude of glufosinate residues. The reason that we
are requesting independent sampling and gas chromatography analyses be
conducted besides that performed by Aventis and its contractors is the
potential for higher glufosinate residue concentrations to be confirmed
above the 0.74 ppm level in rice grain and 1.48 ppm level in rice straw
when sampled at 70 days or more after the last treatment. We are
concerned that Aventis' sampling protocol may have been biased in some
unidentified manner and that samples above the 0.74 ppm level in rice
grain and 1.48 ppm level in rice straw were missed in the field residue
trials. While EPA emphasizes that the treatment regime was selected to
represent the use pattern that is the most likely to result in the
highest residues, we are concerned that sampling bias may have
transpired and resulted in bias in the G.C. analyses. We are also
concerned that glufosinate treatment may have occurred closer to the
sampling period than is the case and higher glufosinate concentrations
were missed. After all, a higher concentration factor of approximately
2.3 was found for rice hulls compared to the grain and straw. We also
question that the finding that no detectable concentration of the
residues occurred when rice whole grain was processed into polished
grain and bran, whereas a glufosinate residue concentration may have
been present at less than the 0.05 ppm (50 ppb) detection limit.
Agency response. The rice magnitude of the residue (15 field trials
conducted throughout the rice growing regions in the United States; 2
composite samples collected at each site) and processing studies were
conducted according to the regulatory guideline requirements (OPPTS
860.1500 and 860.1520) and conformed to EPA GLP Standards. It is
difficult to further address the potential for bias since the comment
gave no specific criteria for the concern. The comment does make
reference to the processing study and the concentration of residues in
rice hull and the lack of concentration of residues in rice bran and
polished rice. The following paragraph is a summary of the rice
processing study.
Processing studies are required to determine if residues reduce or
concentrate during food processing (processing factor = concentration
in processed commodity / concentration in unprocessed commodity).
Processing factors are dependent on several factors including the
location of the residues (surface or translocated residues), loss of
water as in dried commodities, and/or the physical chemical properties
of the residues. The rice processing study (conducted at 5x the
proposed rate) resulted in quantifiable concentrations of glufosinate
ammonium, N-acetyl-glufosinate, and 3-MP in/on all commodities
excluding glufosinate ammonium and N-acetyl-glufosinate in/on rice hull
(residues at the LOQ assumed for calculation of processing factor).
Based on the combined glufosinate ammonium, N-acetyl-glufosinate, and
3-MP residues in/on the processed and unprocessed commodities, the
following processing factors were calculated: rice hull--2.8x, rice
bran--0.9x, and polished rice--1.3x. The dietary analyses assumed
average field trial residues and a processing factor of 1.3 for all
rice commodities excluding rice bran where a processing factor of 0.9
was assumed (rice hull is not a human food commodity).
4. Comment--acute toxicity. EPA states that glufosinate ammonium
has been classified as toxicity category III for acute oral, dermal,
and inhalation toxicity; and for eye irritation. EPA finds that
glufosinate ammonium is not a dermal irritant (toxicity category IV)
nor is it a dermal sensitizer. The oral LD50 is 2 g/kg in
male rats, and 1.62 g/kg in female rats. But we are concerned about
acute toxicity because of the published finding that glufosinate causes
convulsions in humans and experimental rodents by brain cell glutamate
receptor activation (glufosinate and glutamate are structurally
similar) according to Matsumura et al. Has EPA considered the
structural similarities between glufosinate and glutamate receptor
activation. We request that EPA review all of the relevant
toxicological literature on human and rat brain cell glutamate receptor
activation and speak with scientists who performed this research as to
the significance of glufosinate tampering with glutamate receptors.
Evidence also exists that glufosinate stimulates nitric oxide
production in the brain through N-methyDaspartate (NMDA) receptors. We
request that EPA investigate this published finding to determine if the
requested herbicide tolerance concentrations are set too high which, is
a possibility.
Agency response. EPA has evaluated both the published and
petitioner submitted toxicity studies. The oral, dermal, and inhalation
toxicity categories assigned by EPA are based on studies conducted
according to the EPA toxicity testing guidelines and were conducted in
compliance with EPA GLP. In an acute oral toxicity study in rats, the
oral LD50 was found to be 1,620 and 2,000 mg/kg/day in
female and male rats, respectively. In this study, no effects were seen
in rats at doses up to 630 mg/kg/day.
The commenter cites two acute exposure studies. Matsumura et al.
have shown that an acute dose of 80 mg/kg injected intraperitoneally
into mice was convulsive and that this effect was partially antagonized
by NMDA antagonists, suggesting that NMDA receptors may mediate this
effect. Nakaki et al. found that injection of glufosinate ammonium
directly into the brain stimulated nitric oxide production as a result
of stimulation of NMDA receptors in rat brain, another neurochemical
effect. But neither of these published studies provide sufficient
appropriate evidence to establish an acute endpoint for risk assessment
from oral, dermal, or inhalation exposures because the routes that they
used, intraperitoneal injection or direct injection into the brain, are
not directly relevant to potential routes of human exposure to
pesticides, i.e., oral, dermal, or inhalation exposure.
The herbicidal mechanism of action of glufosinate ammonium is
inhibition of the enzyme glutamine synthetase. This enzyme is also
present in mammalian systems. In mammals, glutamine synthetase
facilitates the conversion of glutamate and ammonia to glutamine and is
therefore involved in the metabolism of nitrogen and ammonia. In
addition, glutamate is a major excitatory neurotransmitter in the
nervous system; inhibition of glutamine synthetase has been shown to
impair its ability to serve as a neuroprotectant by controlling
glutamate concentrations in neurons. More generally in the body,
ammonia is buffered for extracellular transport through its interaction
with glutamate to form glutamine by glutamine synthetase.
EPA also reviewed mechanistic studies submitted by the petitioner
as well as the published studies, and, where applicable and
appropriate, incorporated findings from these studies in the human
health risk assessment. In fact, the intermediate-term and long-term
incidental oral endpoints and the chronic dietary endpoint are based on
brain glutamine synthetase inhibition, the most sensitive indicator of
glufosinate ammonium toxicity in humans and experimental animals.
[[Page 55844]]
After reviewing all of the submitted data, EPA confirms that the
tolerances, as proposed, are safe.
5. Comment--genotoxicity. EPA claims that ... based on results of a
complete genotoxicity data base, there is no evidence of mutagenic
activity in a battery of studies, including: Salmonella spp., E. coli,
in vitro mammalian cell gene mutation assays, mammalian cell chromosome
aberration assays, in vivo mouse bone marrow micronucleus assays, and
unscheduled DNA synthesis assays. EPA needs to inquire with the FDA,
USDA, ATSDR, medical doctors and scientists as to whether there are
reports of glufosinate induced mutations and gene toxicity which appear
to be glossed over in the Aventis petition.
Agency response. Glufosinate ammonium was clearly negative in the
acceptable guideline mutagenicity studies. The test battery included: a
Salmonella typhimurium and Escherichia coli reverse gene mutation
assay, in vitro mammalian cell gene mutation and chromosome aberration
assays, in vivo mouse bone marrow micronucleus assay and an in vitro
unscheduled DNA synthesis assay. All studies were performed in
accordance with the specified Office of Prevention, Pesticides, and
Toxic Substances (OPPTS) Harmonized Mutagenicity Test Guidelines Series
870 and satisfied the testing requirements of the Federal Insecticide,
Fungicide, and Rodenticide Act (FIFRA), the Toxic Substances Control
Act (TSCA), and the Organization for Economic Cooperation and
Development (OECD). Further, each study meets the requirement of 40 CFR
part 160, Good Laboratory Practice (GLP) and was subjected to a Quality
Assurance(QA) inspection. Based on the negative responses observed in
these assays, EPA concluded that there is no concern for mutagenicity
from exposure to glufosinate ammonium. In addition, no evidence of
carcinogenicity was observed in mice and rats in acceptable guideline
carcinogenicity studies. As indicated previously, EPA evaluated both
petitioner submitted guideline studies and published scientific
studies. In addition, the petitioner is required by law under FIFRA
(6)(a)2) to report any adverse finding to EPA.
No mutagenicity studies were found in the open literature and the
Agency for Toxic Substances and Disease Registry (ATSDR) has no
finalized, draft, or ``under development'' toxicological profile for
glufosinate ammonium. Finally, FDA has evaluated the human safety of
multiple crops with resistance to glufosinate ammonium and has no
concerns for human safety but has no mutagenicity or toxicity data in
the Biotechnology Notification Files on this herbicide.
6. Comment--reproductive and developmental toxicity. We are
skeptical of EPA's findings because, based on peer-reviewed studies in
the published literature, birth defects have been caused by exposure of
the human father to the herbicide. EPA needs to thoroughly investigate
these findings and reconsider the glufosinate herbicide tolerance
limits requested by Aventis as entirely unsafe and unacceptably high.
It is rather distressing to note that there does not seem to be peer
reviewed studies on the metabolism of the high levels of acetyl
glufosinate in harvested GM crops to highly neurotoxic and teratogenic
glufosinate. Certainly, gut bacteria are well known to contain enzymes
that remove acetyl groups from glufosinate and mammalian enzymes may
also be capable of removing the acetyl group from glufosinate. Even
though glufosinate is being used widely with GM crops in North America
its safety is far from proven and its impact on humans and farm animals
is difficult to trace because the GM products are not labeled for
consumption. We request that EPA obtain more technical data and
information to better define the neurotoxicity and teratogenicity of
glufosinate and its metabolites, especially in humans. Glufosinate, for
example, was found to trigger apoptosis (programmed cell suicide) in
the developing brain of the embryonic mouse. Numerous, well established
studies showing brain damage and birth defects seem to have been
ignored by those regulating use of the herbicide. We request that the
EPA conduct a more comprehensive investigation of available literature
on glufosinate and make requests for unpublished information from
independent scientists such as their expert opinions on the adverse
health effects of glufosinate and its metabolites.
We request the same under subchronic, chronic, animal metabolism,
and metabolite toxicology as requested for Reproductive and
Developmental toxicity.
Agency response. The study authors (cited study by Garcia et al)
state in their conclusion that ``these findings warrant further
investigation.'' In this study, only 16 individuals out of 261
referenced glufosinate ammonium. The results of this study indicated
that there was a marginally significant increased risk of paternally
related developmental toxicity. However, in this study various
contributing factors such as smoking, work habits etc. were not
evaluated and therefore, this epidemiological evaluation does not
establish a causal definitive link to paternally related developmental
toxicity. The potential for glufosinate ammonium to cause developmental
or reproductive effects due to exposure (male or female) has been
evaluated in acceptable guideline studies in rats and rabbits. Based on
these studies, glufosinate ammonium is not teratogenic in rats and
rabbits.
The petitioner has submitted acute, subchronic, chronic,
developmental, and reproductive toxicity studies conducted with
glufosinate ammonium. The petitioner has also submitted developmental
toxicity studies (rat and rabbit) and subchronic studies (rat, mouse,
and dog) with N-acetyl-glufosinate and 3-MP. All of these studies were
conducted according to the regulatory guideline requirements (OPPTS 870
series) and conformed to EPA GLP Standards. EPA has reviewed all of
these studies and selected the most sensitive endpoints. Based on a
comparison of the common studies conducted with the parent and
metabolites, the metabolites exhibited toxic effects at doses equal to
or greater than the parent and EPA concluded that N-acetyl-glufosinate
and 3-MP are not likely to be more toxic than glufosinate ammonium. In
regards to the enzyme that can remove acetyl groups from substrates,
these enzymes are present in the toxicology test systems used to
evaluate the parent and metabolites.
In the cited study by Watanabe, mouse embryo cultures were exposed
to glufosinate ammonium. This is an in vitro experiments which indicate
apoptosis in the developing brain of cultured mouse embryos. It should
be noted that apoptosis is a normal part of the brain development
process. This experiments did not use whole animals and the current
scientific knowledge is not sufficient to allow extrapolation of in
vitro results to whole animals.
7. Comment--endocrine disruption. We find EPA's statements on the
potential of glufosinate to function as an endocrine-disrupting
substance in humans and animals as not founded on logical information
or peer-reviewed studies. In fact EPA states that no special studies
have been conducted to investigate the potential of glufosinate
ammonium to induce estrogenic or other endocrine effects. Given the
enormous complexities of mammalian hormonal regulatory systems and the
current uncertainties existing in this field of knowledge as revealed
by EPA's Endocrine Disruptor Advisory Committee several years ago about
how to screen for potential endocrine-disrupting substances, we feel
it's totally premature for EPA at this time to dismiss all concerns
about glufosinate
[[Page 55845]]
as an endocrine-disrupting substance. EPA stresses that no evidence of
estrogenic or other endocrine effects have been noted in any of the
toxicology studies that have been conducted with this product and there
is no reason to suspect that any such effects would be likely. Due to
the millions of Americans and their children exposed to glufosinate and
its metabolites, EPA needs to conclusively determine if this herbicide
has endocrine-disrupting potential.
Agency response. EPA is required under the FFDCA, as amended by the
FQPA, to develop a screening program to determine whether certain
substances, including all pesticide active and other ingredients, ``may
have an effect in humans that is similar to an effect produced by a
naturally occurring estrogen, or other such endocrine effects as the
Administrator may designate.'' Following the recommendations of its
Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC),
EPA determined that there was scientific bases for including, as part
of the program, the androgen and thyroid hormone systems, in addition
to the estrogen hormone system. EPA also adopted EDSTAC's
recommendation that the Program include evaluations of potential
effects in wildlife. For pesticide chemicals, EPA will use Federal
Insecticide, Fungicide and Rodenticide Act (FIFRA) and, to the extent
that effects in wildlife may help determine whether a substance may
have an effect in humans, FFDCA has authority to require the wildlife
evaluations. As the science develops and resources allow, screening of
additional hormone systems may be added to the Endocrine Disruptor
Screening Program (EDSP).
When the appropriate screening and/or testing protocols being
considered under the Agency's EDSP have been developed, glufosinate
ammonium may be subjected to additional screening and/or testing to
better characterize effects related to endocrine disruption. The
studies submitted as guideline studies as well as the data reviewed in
the open literature did not provide any obvious indications that
glufosinate ammonium and/or its metabolites have specific endocrine
disruptive effects.
8. Comment--dietary exposure. EPA states that tolerances have been
established (40 CFR 180.473) for the combined residues of glufosinate
ammonium and metabolites in or on a variety of RACs. EPA further
maintains that no appropriate toxicological endpoint attributable to a
single exposure was identified in the available toxicity studies. This
is why EPA has not established an acute RfD for the general population
including infants and children. An acute RfD of 0.063 mg/kg/day was
established, however, for the females 13+ subgroup. Therefore, an acute
dietary analysis was conducted for this sub-population; whereas,
chronic dietary analysis was conducted for the usual populations. We
request that EPA reconsider and reevaluate the health information
finding that no appropriate toxicological endpoint attributable to a
single exposure was identified in the available toxicity studies as too
being limited and erroneous.
Agency response. EPA has evaluated the published toxicity studies
and considered the relevant petitioner submitted studies. On the basis
of these studies, no appropriate endpoint of concern attributable to a
single exposure was identified. EPA has asked the petitioner to conduct
a study to evaluate potential effects of glufosinate ammonium following
a single exposure (acute effects) with glutamate synthetase
measurements. Until such data are available, EPA has applied additional
data base UF to account or allow for uncertainty about those potential
effects of acute exposure.
9. Comment--infants and children. We are very concerned that EPA
finds that the toxicological data base is sufficient for evaluating
prenatal and postnatal toxicity for glufosinate ammonium in human
infants and children using exclusively results from rats and rabbits.
Although EPA states that there are no prenatal or postnatal
susceptibility concerns for infants and children, based on the results
of the rat and rabbit developmental toxicity studies and the 2-
generation reproduction study, we are concerned that human infants and
children may possess genetic predispositions, biochemical
individualities and behavioral patterns very different from rats and
rabbits. EPA needs to do a more thorough literature review and
interview scientists and medical doctors who may have relevant
information on the prenatal and postnatal toxicity for glufosinate
ammonium in human infants and children.
As EPA notes, Based on clinical signs of neurological toxicity in
short and intermediate dermal toxicity studies with rats, the agency
has determined that an added FQPA safety factor of 3x is appropriate
for assessing the risk of glufosinate ammonium derived residues in crop
commodities. Using the conservative assumptions described in the
exposure section above, the percent of the chronic RfD that will be
used for exposure to residues of glufosinate ammonium in food for
children 1-6 (the most highly exposed sub-group) is 61%. Infants
utilize 37% of the chronic RfD. As in the adult situation, drinking
water levels of comparison are higher than the worst case DWECs and are
expected to use well below 100% of the RfD, if they occur at all.
Therefore, there is a reasonable certainty that no harm will occur to
infants and children from aggregate exposure to residues of glufosinate
ammonium.
Agency response. The short-term (dermal, inhalation, and incidental
oral) and acute dietary (females 13-50 years) endpoints are based on
reduced fetal body weight and increased fetal death seen in the rabbit
developmental toxicity study (6.3 mg/kg/day). An acute dietary endpoint
for the general population, including infants and children, could not
be identified due to no adverse effects seen in the relevant studies.
The chronic dietary endpoint is based on a weight-of-evidence approach
from several studies which demonstrated brain glutamine synthetase
inhibition and alterations in the electrocardiogram (6.0 mg/kg/day).
EPA concluded that the toxicological data base for glufosinate ammonium
was not complete and requested the submission of the following studies:
(1) Acute neurotoxicity study conducted in the rat which includes
glutamine synthetase activity measurement in the liver, kidneys, and
brain; (2) a developmental neurotoxicity (DNT) study conducted in the
rat which includes comparative glutamine synthetase activity
measurement in the liver, kidneys, and brain of the pups and mothers;
and (3) a 28-day inhalation toxicity study in rats with glutamine
synthetase activity measurements in brain, kidney, liver and lung. EPA
also requested additional data to confirm that liver and kidney
changes, observed in the absence of histopathological changes, are an
adaptive response and not an adverse effect. Kidney and liver function
assays should be performed in addition to glutamine synthetase activity
measurements. Pending the submission of the requested data, a 10x data
base uncertainty factor was applied to all oral and dermal risk
assessments and a 100x uncertainty factor was applied to all inhalation
risk assessments. These uncertainty factors combined with the
traditional 100x inter/intra species uncertainty factor, resulted in a
total uncertainty factor of 1,000x for dermal and oral exposure
assessments and 3,000x for inhalation exposure assessments (10,000x
uncertainty factor reduced to 3,000x based on Agency policy cited in
Unit III.B.).
[[Page 55846]]
EPA concluded that there is no qualitative or quantitative evidence
of increased susceptibility in the developmental toxicity study
conducted in rats. Qualitative evidence of increased susceptibility is
demonstrated in the rabbit developmental toxicity study since fetal
deaths were observed in the presence of lesser maternal toxicity at the
same dose. There is also quantitative evidence of increased
susceptibility in the rat 2-generation reproduction study. In this
study, a decrease in the number of viable pups was observed in the
absence of parental toxicity at any dose. Since there is qualitative
evidence of increased susceptibility of the young following exposure to
glufosinate ammonium, EPA performed a degree of concern analysis to:
(1) Determine the level of concern for the effects observed when
considered in the context of all available toxicity data; and (2)
identify any residual uncertainties after establishing toxicity
endpoints and traditional uncertainty factors to be used in the risk
assessment of this chemical. Based on the data gaps listed above, the
EPA did not identify any other residual uncertainties. The established
endpoints are protective of pre-/postnatal toxicity following acute and
chronic exposures.
The Notice of Filing (NOF) published in the Federal Register of
July 24, 2002 (67 FR 48465)(FRL-7184-6) represents a summary of the
petition prepared by the petitioner and represents the views of the
petitioner. As such, and in this case, discrepancies may arise between
what is stated in the NOF and the procedures/conclusions employed by
EPA when assessing human health risk. For instance, the toxicological
data base for glufosinate ammonium has been reevaluated by EPA since
July 2002, and some of the conclusions presented in the NOF concerning
the toxicity of glufosinate ammonium do not reflect current EPA
conclusions.
10. Comment--cumulative effects section 408(b)(2)(D)(v). We are
deeply concerned about the potential for cumulative effects of
glufosinate and its metabolites, and therefore request that EPA not
approve the Aventis tolerance petition unless or until peer-reviewed
confirming scientific evidence is available that glufosinate and its
metabolites do not cause any cumulative effects. It is not acceptable
public health policy to dismiss cumulative effects of glufosinate and
its metabolites because of lack of scientific evidence and lack of any
studies. Law requires that, when considering whether to establish,
modify, or revoke a tolerance, the EPA must consider ``available
information'' concerning the cumulative effects of a particular
pesticide's residues and ``other substances that have a common
mechanism of toxicity.'' EPA has indicated that, at this time, the
Agency does not have available data to determine whether glufosinate
ammonium has a common mechanism of toxicity with other substances or
how to include this pesticide in a cumulative risk assessment. Unlike
other pesticides for which EPA has followed a cumulative risk approach
based on a common mechanism of toxicity, EPA suggests that glufosinate
ammonium does not appear to produce a toxic metabolite produced by
other substances. For the purposes of this tolerance petition,
therefore, it has not been assumed that glufosinate ammonium has a
common mechanism of toxicity with other substances. We disagree with
EPA's illogical and unscientific assumption that glufosinate ammonium
has a common mechanism of toxicity with other substances. We propose
that further study is necessary to conclusively confirm such an
assumption.
Agency response. Section 408(b)(2)(D)(v) of the FFDCA requires
that, when considering whether to establish, modify, or revoke a
tolerance, the Agency consider ``available information'' concerning the
cumulative effects of a particular pesticide's residues and ``other
substances that have a common mechanism of toxicity.''
EPA does not have, at this time, sufficient data to determine
whether glufosinate ammonium has a common mechanism of toxicity with
other substances. Unlike other pesticides for which EPA has followed a
cumulative risk approach based on a common mechanism of toxicity (i.e.,
organophosphates), EPA has not made a common mechanism of toxicity
finding as to glufosinate ammonium and any other substances and
glufosinate ammonium does not appear to produce a toxic metabolite
produced by other substances. For the purposes of this tolerance
action, therefore, EPA has not assumed that glufosinate ammonium has a
common mechanism of toxicity with other substances. For information
regarding EPA's efforts to determine which chemicals have a common
mechanism of toxicity and to evaluate the cumulative effects of such
chemicals, see the policy statements released by EPA's Office of
Pesticide Programs concerning common mechanism determinations and
procedures for cumulating effects from substances found to have a
common mechanism on EPA's website at http://www.epa.gov/pesticides/cumulative/
.
11. Comment--safety determination U.S. population. We believe that
EPA has not done an adequate scientific job with respect to its safety
determination for the U.S. population. By using what EPA claims (and
may be a flawed set of assumptions) are the conservative assumptions
described above and based on the completeness and reliability of the
toxicity data, it is concluded that chronic dietary exposure to the
registered and proposed uses of glufosinate ammonium will utilize at
most 25% of the chronic RfD for the U.S. population. We disagree with
EPA's assumption that the actual exposure is likely to be significantly
less than predicted by this analysis as data and models that are more
realistic are developed. We disagree with EPA's assumption that
exposures below 100% of the reference dose (RfD) are generally assumed
to be of no concern because the RfD represents the level at or below
which daily aggregate exposure over a lifetime will not pose
appreciable risk to human health. We dispute that the acute population
of concern, female 13+ utilizes 34% of the acute RfD. We disagree with
EPA's assumption that this is a Tier One highly conservative assessment
and actual exposure is likely to be far less. Drinking water levels of
comparison based on dietary exposures are greater than highly
conservative estimated levels, and would be expected to be well below
the 100% level of the RfD, if they occur at all, assuming that EPA's
set of assumptions are reasonably accurate which they may not be. We
believe that EPA has erroneously concluded that it is not appropriate
to aggregate non-dietary exposures with dietary exposures in a risk
assessment because the toxicity end-points are different. We strongly
dispute EPA's concluding assumption that there is a reasonable
certainty that no harm will occur to the U.S. population from aggregate
exposure (food, drinking water and nonresidential) to residues of
glufosinate ammonium and metabolites.
Agency response. Contrary to what was written in the Notice of
Filing prepared by the petitioner, EPA did aggregate dietary (food +
drinking water) and residential exposures. Glufosinate ammonium is
currently registered for application in the residential setting for
lawn renovation and spot treatment purposes. Since the lawn renovation
use resulted in exposures greater than EPA's level of concern,
revocation of this use was recommended. Therefore, aggregate exposures
were conducted by combining dietary exposure and residential exposure
resulting from the spot treatment use. The resulting
[[Page 55847]]
combined exposures were subtracted from the appropriate dose and
drinking water levels of comparison (DWLOCs) were calculated and
compared to EECs in groundwater and surface water. The EECs were
generated using SCIGROW (groundwater) and PRZM-EXAMS (surface water).
SCIGROW is a regression model designed to estimate a screening level of
a pesticide concentration at an agricultural site which is highly
vulnerable to leaching due to permeable soil overlaying shallow ground
water. PRZM-EXAMS is used to estimate concentration that might occur in
vulnerable surface water (assumes 87% of the basin is cropped and
entire cropped area is treated). Both models assumed 3 applications at
1.5 lbs ai/acre (highest registered/proposed rate). The resulting EECs
were less than the DWLOCs indicating aggregate exposures are less than
EPA's level of concern.
12. Comment. Additional issues not apparently being addressed by
EPA such as negative impacts on beneficial insects. Bystander or
beneficial insects have been detrimentally effected by the herbicide.
Kutlesa and Caveny found that the herbicide had a number of neurotoxic
impacts on the skipper butterfly at levels of herbicide experienced in
the field. Ahn et al found that glufosinate was toxic to some but not
all predatory insects at levels of the herbicide experienced in the
field. Studies showing that helpful predatory insects or bystander
insects are poisoned by the herbicide seem to have been ignored by
regulators of the herbicide.
Agency response. This comment raises an issue concerning the
pesticide's registrability under FIFRA and is not directly relevant to
the safety determination under FFDCA. For registrations of a pesticide
under FIFRA, EPA requires non-target insect data if the proposed use
will result in exposure to honey bees (40 CFR 158.590). Two studies on
the toxicity of glufosinate ammonium to bees indicates that the
herbicide (technical and a formulated product) is practically non-toxic
to bees via contact and oral routes. The cited studies suggest that
glufosinate ammonium may cause mortality to insects, other than bees,
and mites may also be affected. The issues of the hazard to non-target
insects will be addressed via registration under FIFRA.
13. Comment. Additional issues not apparently being addressed by
EPA such as glufosinate residues in other crop varieties. Muller et al
studied glufosinate metabolites in transgenic and unmodified sugar
beet, carrot, purple foxglove and thorn apple, and they found that
unmodified (i.e., non-genetically engineered) crops contained
glufosinate mainly while GM crops contained higher levels of
glufosinate and acetyl glufosinate. Beriault et al studied phloem
transport of glufosinate and acetylglufosinate in canola in GM canola
and unmodified canola and found that both chemicals were highly mobile.
Agency response. Common toxicity studies conducted with glufosinate
ammonium, N-acetyl-glufosinate, and 3-MP indicate that N-acetyl-
glufosinate and 3-MP exhibit toxic effects at doses equal to or greater
than glufosinate ammonium. Based on these toxicity studies, EPA
concluded that N-acetyl-glufosinate, and 3-MP are not likely to be more
toxic than glufosinate ammonium (risk assessment assumes they are of
equal toxicity to parent). The field trial data were submitted for the
transgenic crops monitored for residues of glufosinate ammonium, N-
acetyl-glufosinate, and 3-MP in/on all food/feed commodities.
Therefore, the higher residues in transgenic crops and/or greater
mobility of the residues of concern has been taken into consideration.
14. Comment. Two hundred and twenty four comments were received
that were opposed to establishing tolerances for glufosinate ammonium
in genetically engineered (GE) rice and cotton. They included some or
all of the following comments from the campaign to halt the
introduction of GE Crops:
I am writing in reference to Bayer CropScience's August 15th
petition to establish a tolerance for Glufosinate in or on Rice and
cotton. I believe that by approving the residues requested by Bayer
you will be exposing the public to unnecessary health risks,
potentially increasing use of toxic herbicides on rice and cotton,
and endangering the livelihoods of farmers by shutting off valuable
export markets that are rejecting transgenic crops. I am concerned
about the loss of overseas markets for farmers growing transgenic
crops and for farmers whose own ability to market their crops is
threatened by genetic pollution. Many countries throughout the world
are refusing transgenic crops and USDA organic standards strictly
prohibit the use of transgenic seeds. Glufosinate tolerance levels
have not been established by the international food standards
commission, Codex Alimentarius. Events such as StarLink and last
year's ProdiGene incident highlight the inadequacies of our current
system in keeping transgenic crops segregated. In Canada, farmers
growing transgenic crops have detected triple herbicide resistance
in weeds and volunteer canola plants as a result of gene transfer,
rendering the herbicides useless. If Bayer's petition is approved,
it will only be a matter of time before red rice, which is the same
species as cultivated rice and also one of the most virulent weeds
on rice farms, becomes resistant to Glufosinate. Similar gene
transfer in rice will lead to the need for new, more toxic
herbicides. Peer-reviewed scientific studies have shown Glufosinate
to be ``highly toxic'' to aquatic animals such as clams, oysters,
water fleas, fish and birds at doses as low as 0.5 ppm. As rice is
grown in an aquatic environment, the adoption of Glufosinate
tolerant rice will have tragic impacts for the ecosystems of rice
growing areas. The EPA classifies Glufosinate as ``persistent'' and
it has been found in the edible parts of spinach, wheat and radishes
more than 120 days after being sprayed with the chemical. The
approval of Glufosinate tolerant rice and cotton will send us a step
backward in our efforts toward a more sustainable agriculture.
Please take action to ensure that our current system of agriculture
moves toward one that is less reliant on chemicals, and ensures our
farmers a prosperous livelihood. I strongly urge you to deny Bayer's
request for approval of Glufosinate tolerance and to work with other
government agencies to enact a more rigorous approval and testing
process for transgenic crops.
Forty one comments were in favor of establishing the tolerances for
glufosinate ammonium. They stated that growers need the new technology
to control weed species.
Agency Response. EPA has concluded that there is a reasonable
certainty that no harm will result to the general population, and to
infants and children from aggregate exposure to glufosinate-ammonium
and its metabolites from established and proposed tolerances. The
issues of the hazard to non-target organisms and crop resistance will
be addressed via registration under FIFRA. The growing of Herbicide
Tolerant crops and potential effects on shipment of crops overseas is
addressed by USDA and FDA in their pre-marketing review of Plant-
Incorporated Protectant Seeds. EPA is responsile for the safety of the
pesticide to be applied to the growing crop.
VII. Objections and Hearing Requests
Under section 408(g) of the FFDCA, as amended by the FQPA, any
person may file an objection to any aspect of this regulation and may
also request a hearing on those objections. The EPA procedural
regulations which govern the submission of objections and requests for
hearings appear in 40 CFR part 178. Although the procedures in those
regulations require some modification to reflect the amendments made to
the FFDCA by the FQPA, EPA will continue to use those procedures, with
appropriate adjustments, until the necessary modifications can be made.
The new section 408(g) of the FFDCA provides essentially the same
process for persons to ``object'' to a regulation for an exemption from
the requirement
[[Page 55848]]
of a tolerance issued by EPA under new section 408(d) of FFDCA, as was
provided in the old sections 408 and 409 of the FFDCA. However, the
period for filing objections is now 60 days, rather than 30 days.
A. What Do I Need to Do to File an Objection or Request a Hearing?
You must file your objection or request a hearing on this
regulation in accordance with the instructions provided in this unit
and in 40 CFR part 178. To ensure proper receipt by EPA, you must
identify docket ID number OPP-2003-0058 in the subject line on the
first page of your submission. All requests must be in writing, and
must be mailed or delivered to the Hearing Clerk on or before November
28, 2003.
1. Filing the request. Your objection must specify the specific
provisions in the regulation that you object to, and the grounds for
the objections (40 CFR 178.25). If a hearing is requested, the
objections must include a statement of the factual issues(s) on which a
hearing is requested, the requestor's contentions on such issues, and a
summary of any evidence relied upon by the objector (40 CFR 178.27).
Information submitted in connection with an objection or hearing
request may be claimed confidential by marking any part or all of that
information as CBI. Information so marked will not be disclosed except
in accordance with procedures set forth in 40 CFR part 2. A copy of the
information that does not contain CBI must be submitted for inclusion
in the public record. Information not marked confidential may be
disclosed publicly by EPA without prior notice.
Mail your written request to: Office of the Hearing Clerk (1900C),
Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460-0001. You may also deliver your request to the
Office of the Hearing Clerk in Rm.104, Crystal Mall 2, 1921
Jefferson Davis Hwy., Arlington, VA. The Office of the Hearing Clerk is
open from 8 a.m. to 4 p.m., Monday through Friday, excluding legal
holidays. The telephone number for the Office of the Hearing Clerk is
(703) 603-0061.
2. Tolerance fee payment. If you file an objection or request a
hearing, you must also pay the fee prescribed by 40 CFR 180.33(i) or
request a waiver of that fee pursuant to 40 CFR 180.33(m). You must
mail the fee to: EPA Headquarters Accounting Operations Branch, Office
of Pesticide Programs, P.O. Box 360277M, Pittsburgh, PA 15251. Please
identify the fee submission by labeling it ``Tolerance Petition Fees.''
EPA is authorized to waive any fee requirement ``when in the
judgement of the Administrator such a waiver or refund is equitable and
not contrary to the purpose of this subsection.'' For additional
information regarding the waiver of these fees, you may contact James Tompkins by phone at (703) 305-5697, by e-mail at tompkins.jim@epa.gov,
or by mailing a request for information to Mr. Tompkins at Registration
Division (7505C), Office of Pesticide Programs, Environmental
Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001.
If you would like to request a waiver of the tolerance objection
fees, you must mail your request for such a waiver to: James Hollins,
Information Resources and Services Division (7502C), Office of
Pesticide Programs, Environmental Protection Agency, 1200 Pennsylvania
Ave., NW., Washington, DC 20460-0001.
3. Copies for the Docket. In addition to filing an objection or
hearing request with the Hearing Clerk as described in Unit VII.A., you
should also send a copy of your request to the PIRIB for its inclusion
in the official record that is described in Unit I.B.1. Mail your
copies, identified by docket ID number OPP-2003-0058, to: Public
Information and Records Integrity Branch, Information Resources and
Services Division (7502C), Office of Pesticide Programs, Environmental
Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001. In person or by courier, bring a copy to the location of the
PIRIB described in Unit I.B.1. You may also send an electronic copy of your request via e-mail to: opp-docket@epa.gov. Please use an ASCII
file format and avoid the use of special characters and any form of
encryption. Copies of electronic objections and hearing requests will
also be accepted on disks in WordPerfect 6.1/8.0 or ASCII file format.
Do not include any CBI in your electronic copy. You may also submit an
electronic copy of your request at many Federal Depository Libraries.
B. When Will the Agency Grant a Request for a Hearing?
A request for a hearing will be granted if the Administrator
determines that the material submitted shows the following: There is a
genuine and substantial issue of fact; there is a reasonable
possibility that available evidence identified by the requestor would,
if established resolve one or more of such issues in favor of the
requestor, taking into account uncontested claims or facts to the
contrary; and resolution of the factual issues(s) in the manner sought
by the requestor would be adequate to justify the action requested (40
CFR 178.32).
VIII. Statutory and Executive Order Reviews
This final rule establishes a tolerance under section 408(d) of the
FFDCA in response to a petition submitted to the Agency. The Office of
Management and Budget (OMB) has exempted these types of actions from
review under Executive Order 12866, entitled Regulatory Planning and
Review (58 FR 51735, October 4, 1993). Because this rule has been
exempted from review under Executive Order 12866 due to its lack of
significance, this rule is not subject to Executive Order 13211,
Actions Concerning Regulations That Significantly Affect Energy Supply,
Distribution, or Use (66 FR 28355, May 22, 2001). This final rule does
not contain any information collections subject to OMB approval under
the Paperwork Reduction Act (PRA), 44 U.S.C. 3501 et seq., or impose
any enforceable duty or contain any unfunded mandate as described under
Title II of the Unfunded Mandates Reform Act of 1995 (UMRA) (Public Law
104-4). Nor does it require any special considerations under Executive
Order 12898, entitled Federal Actions to Address Environmental Justice
in Minority Populations and Low-Income Populations (59 FR 7629,
February 16, 1994); or OMB review or any Agency action under Executive
Order 13045, entitled Protection of Children from Environmental Health
Risks and Safety Risks (62 FR 19885, April 23, 1997). This action does
not involve any technical standards that would require Agency
consideration of voluntary consensus standards pursuant to section
12(d) of the National Technology Transfer and Advancement Act of 1995
(NTTAA), Public Law 104-113, section 12(d) (15 U.S.C. 272 note). Since
tolerances and exemptions that are established on the basis of a
petition under section 408(d) of the FFDCA, such as the tolerance in
this final rule, do not require the issuance of a proposed rule, the
requirements of the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et
seq.) do not apply. In addition, the Agency has determined that this
action will not have a substantial direct effect on States, on the
relationship between the national government and the States, or on the
distribution of power and responsibilities among the various levels of
government, as specified in Executive Order 13132, entitled
Federalism(64 FR 43255, August 10, 1999). Executive Order 13132
requires EPA to develop an accountable process
[[Page 55849]]
to ensure ``meaningful and timely input by State and local officials in
the development of regulatory policies that have federalism
implications.'' ``Policies that have federalism implications'' is
defined in the Executive order to include regulations that have
``substantial direct effects on the States, on the relationship between
the national government and the States, or on the distribution of power
and responsibilities among the various levels of government.'' This
final rule directly regulates growers, food processors, food handlers
and food retailers, not States. This action does not alter the
relationships or distribution of power and responsibilities established
by Congress in the preemption provisions of section 408(n)(4) of the
FFDCA. For these same reasons, the Agency has determined that this rule
does not have any ``tribal implications'' as described in Executive
Order 13175, entitled Consultation and Coordination with Indian Tribal
Governments (65 FR 67249, November 6, 2000). Executive Order 13175,
requires EPA to develop an accountable process to ensure ``meaningful
and timely input by tribal officials in the development of regulatory
policies that have tribal implications.'' ``Policies that have tribal
implications'' is defined in the Executive order to include regulations
that have ``substantial direct effects on one or more Indian tribes, on
the relationship between the Federal Government and the Indian tribes,
or on the distribution of power and responsibilities between the
Federal Government and Indian tribes.'' This rule will not have
substantial direct effects on tribal governments, on the relationship
between the Federal Government and Indian tribes, or on the
distribution of power and responsibilities between the Federal
Government and Indian tribes, as specified in Executive Order 13175.
Thus, Executive Order 13175 does not apply to this rule.
IX. Congressional Review Act
The Congressional Review Act, 5 U.S.C. 801 et seq., as added by the
Small Business Regulatory Enforcement Fairness Act of 1996, generally
provides that before a rule may take effect, the agency promulgating
the rule must submit a rule report, which includes a copy of the rule,
to each House of the Congress and to the Comptroller General of the
United States. EPA will submit a report containing this rule and other
required information to the U.S. Senate, the U.S. House of
Representatives, and the Comptroller General of the United States prior
to publication of this final rule in the Federal Register. This final
rule is not a ``major rule'' as defined by 5 U.S.C. 804(2).
List of Subjects in 40 CFR Part 180
Environmental protection, Administrative practice and procedure,
Agricultural commodities, Pesticides and pests, Reporting and
recordkeeping requirements.
Dated:September 23, 2003.
Debra Edwards,
Director, Registration Division, Office of Pesticide Programs.
0
Therefore, 40 CFR chapter I is amended as follows:
PART 180--[AMENDED]
0
1. The authority citation for part 180 continues to read as follows:
Authority: 21 U.S.C. 321(q), 346(a) and 371.
0
2. Section 180.473 is revised to read as follows:
Sec. 180.473 Glufosinate ammonium; tolerances for residues.
(a) General. (1) Tolerances are established for residues of the
herbicide glufosinate ammonium (butanoic acid, 2-amino-4-
(hydroxymethylphosphinyl)-, monoammonium salt) and its metabolites, 2-
acetamido-4-methylphosphinico-butanoic acid and 3-methylphosphinico-
propionic acid, expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents, in or on the
following food commodities:
------------------------------------------------------------------------
Commodity Parts per million
------------------------------------------------------------------------
Almond, hulls........................................ 0.50
Apple................................................ 0.05
Banana............................................... 0.30
Banana, pulp......................................... 0.20
Bushberry subgroup 13B............................... 0.15
Cattle, fat.......................................... 0.40
Cattle, meat......................................... 0.15
Cattle, meat byproducts.............................. 6.0
Cotton, gin byproducts............................... 15
Cotton, undelinted seed.............................. 4.0
Egg.................................................. 0.15
Goat, fat............................................ 0.40
Goat, meat........................................... 0.15
Goat, meat byproducts................................ 6.0
Grape................................................ 0.05
Hog, fat............................................. 0.40
Hog, meat............................................ 0.15
Hog, meat byproducts................................. 6.0
Horse, fat........................................... 0.40
Horse, meat.......................................... 0.15
Horse, meat byproducts............................... 6.0
Juneberry............................................ 0.10
Lingonberry.......................................... 0.10
Milk................................................. 0.15
Nut, tree, group 14.................................. 0.10
Potato............................................... 0.80
Potato, chips........................................ 1.60
Potato granules and flakes........................... 2.00
Poultry, fat......................................... 0.15
Poultry, meat........................................ 0.15
Poultry, meat byproducts............................. 0.60
Salal................................................ 0.10
Sheep, fat........................................... 0.40
Sheep, meat.......................................... 0.15
Sheep, meat byproducts............................... 6.0
------------------------------------------------------------------------
(2) Tolerances are established for residues of the herbicide
glufosinate ammonium (butanoic acid, 2-amino-4-
(hydroxymethylphosphinyl)-, monoammonium salt) and its metabolites, 2-
acetamido-4-methylphosphinico-butanoic acid and 3-methylphosphinico-
propionic acid, expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents, in or on the
following food commodities derived from transgenic canola, transgenic
cotton, transgenic field corn, transgenic rice, transgenic soybean and
transgenic sugar beet that are tolerant to glufosinate ammonium:
------------------------------------------------------------------------
Parts per
Commodity million
------------------------------------------------------------------------
Aspirated grain fractions.................................. 25.0
Beet, sugar, molasses...................................... 5.0
Beet, sugar, roots......................................... 0.9
Beet, sugar, tops (leaves)................................. 1.5
Canola, meal............................................... 1.1
Canola, seed............................................... 0.4
Corn, field, forage........................................ 4.0
Corn, field, grain......................................... 0.2
Corn, field, stover........................................ 6.0
Cotton, gin byproducts..................................... 15
Cotton, undelinted seed.................................... 4.0
Rice, grain................................................ 1.0
Rice, hull................................................. 2.0
Rice, straw................................................ 2.0
Soybean.................................................... 2.0
Soybean, hulls............................................. 5.0
------------------------------------------------------------------------
(b) Section 18 emergency exemptions. [Reserved]
(c) Tolerances with regional restrictions. [Reserved]
(d) Indirect or inadvertent residues. [Reserved]
[FR Doc. 03-24565 Filed 9-26-03; 8:45 am]
BILLING CODE 6560-50-S